ArticleFrontiers in molecular biosciences2025
SOX2 induces LPCAT1 expression to promote cholesterol metabolic reprogramming-mediated invasion and metastasis in osteosarcoma.
Article in Frontiers in molecular biosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- LL-37 inhibits osteosarcoma progression by suppressing SQLE-mediated cholesterol synthesis via the PTEN/AKT/mTOR pathway.Journal of bone oncology · 2026Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: SOX2 and LPCAT1 are implicated in tumor progression, but their roles in osteosarcoma pathogenesis and cholesterol metabolism remain unclear. Method: SOX2 and LPCAT1 expression in osteosarcoma tissues and cell lines was assessed via qRT-PCR and Western blot. Functional assays (CCK-8, wound healing and Transwell) evaluated proliferation, migration, and invasion of osteosarcoma cells. SOX2-LPCAT1 binding was confirmed by dual-luciferase reporter assay and ChIP assays. RNA sequencing and bioinformatics analyses explored cholesterol metabolism pathways. Result: SOX2 and LPCAT1 were overexpressed in osteosarcoma. LPCAT1 or SOX2 overexpression promoted malignant behaviors and cholesterol metabolism (free cholesterol/total cholesterol levels, SREBP1/INSIG1 expression) of osteosarcoma cells, while shSOX2 or shLPCAT1 did the opposite. SOX2 transcriptionally activated LPCAT1. LPCAT1 reversed shSOX2-induced suppression, while LPCAT1 knockdown attenuated SOX2-driven oncogenicity. Conclusion: The SOX2/LPCAT1 axis drives osteosarcoma progression by modulating cholesterol metabolism.
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Registered trials
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